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AVR2 靶向 BSL 家族成员,后者作为易感性因素抑制宿主免疫。

AVR2 Targets BSL Family Members, Which Act as Susceptibility Factors to Suppress Host Immunity.

机构信息

Division of Plant Science, School of Life Science, University of Dundee (at JHI), Invergowrie, Dundee DD2 5DA, United Kingdom.

Key Laboratory of Horticultural Plant Biology (HZAU), Ministry of Education, Key Laboratory of Potato Biology and Biotechnology, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, Hubei 430070, China.

出版信息

Plant Physiol. 2019 May;180(1):571-581. doi: 10.1104/pp.18.01143. Epub 2019 Feb 19.

DOI:10.1104/pp.18.01143
PMID:30782963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6501069/
Abstract

To be successful plant pathogens, microbes use "effector proteins" to manipulate host functions to their benefit. Identifying host targets of effector proteins and characterizing their role in the infection process allow us to better understand plant-pathogen interactions and the plant immune system. Yeast two-hybrid analysis and coimmunoprecipitation were used to demonstrate that the effector AVIRULENCE 2 (PiAVR2) interacts with all three BRI1-SUPPRESSOR1-like (BSL) family members from potato (). Transient expression of BSL1, BSL2, and BSL3 enhanced leaf infection. BSL1 and BSL3 suppressed INFESTIN 1 elicitin-triggered cell death, showing that they negatively regulate immunity. Virus-induced gene silencing studies revealed that BSL2 and BSL3 are required for BSL1 stability and show that basal levels of immunity are increased in -silenced plants. Immune suppression by BSL family members is dependent on the brassinosteroid-responsive host transcription factor CIB1/HBI1-like 1. The effector PiAVR2 targets all three BSL family members in the crop plant These phosphatases, known for their role in growth-promoting brassinosteroid signaling, all support virulence and thus can be regarded as susceptibility factors in late blight infection.

摘要

为了成为成功的植物病原体,微生物利用“效应蛋白”来操纵宿主功能,使其受益。鉴定效应蛋白的宿主靶标并描述它们在感染过程中的作用,可以帮助我们更好地理解植物-病原体相互作用和植物免疫系统。酵母双杂交分析和共免疫沉淀实验表明,效应因子 AVIRULENCE 2(PiAVR2)与来自马铃薯的所有三个 BRASSINOSTEROID INSENSITIVE 1-SUPPRESSOR1-LIKE(BSL)家族成员相互作用()。BSL1、BSL2 和 BSL3 的瞬时表达增强了叶片感染。BSL1 和 BSL3 抑制 INFESTIN 1 激发素触发的细胞死亡,表明它们负调控免疫。病毒诱导的基因沉默研究表明,BSL2 和 BSL3 是 BSL1 稳定性所必需的,并且表明在沉默的植物中基础水平的免疫增强。BSL 家族成员的免疫抑制依赖于油菜素类固醇反应性宿主转录因子 CIB1/HBI1-LIKE 1。作物植物中的 效应因子 PiAVR2 靶向所有三个 BSL 家族成员 这些磷酸酶以其在促进生长的油菜素类固醇信号传导中的作用而闻名,都支持 毒性,因此可以被视为晚疫病感染中的易感性因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/80925e5e5c0f/PP_201801143R2_f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/41ddea7f01ad/PP_201801143R2_f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/1f323dbe8cf2/PP_201801143R2_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/9a7742a7095a/PP_201801143R2_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/f0b4c676208a/PP_201801143R2_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/8d7c7fa4c9f2/PP_201801143R2_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/4ea1be28b4be/PP_201801143R2_f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/80925e5e5c0f/PP_201801143R2_f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/41ddea7f01ad/PP_201801143R2_f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/ae9aced437e4/PP_201801143R2_f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/1f323dbe8cf2/PP_201801143R2_f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/9a7742a7095a/PP_201801143R2_f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/f0b4c676208a/PP_201801143R2_f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/8d7c7fa4c9f2/PP_201801143R2_f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/4ea1be28b4be/PP_201801143R2_f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3bc/6501069/80925e5e5c0f/PP_201801143R2_f8.jpg

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